Experimental evidence collected over the past decade has revealed that targeting cyclooxygenase-2 (COX-2) may have some efficacy for chemoprevention of cancer. However, recent safety concerns over the long-term use of COX-2 selective inhibitors are prompting research aimed at identifying other specific targets downstream of COX-2. In this regard, several groups have found that NSAIDs and COX-2 selective inhibitors primarily reduce the production of prostaglandin (PG) E2, a biologically active lipid product of the COX-2 enzyme, which results in attenuation of PGE2 signaling in the tumor microenvironment. Therefore, a detailed understanding of the PGE 2 signaling pathway in transformed cells is critical to help identify novel and safer targets for effective prevention and/or treatment of cancer. Here we review the recent advances in elucidating the molecular mechanisms by which PGE2 promotes carcinogenesis.
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